The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

RASD1  -  RAS, dexamethasone-induced 1

Homo sapiens

Synonyms: AGS1, Activator of G-protein signaling 1, DEXRAS1, Dexamethasone-induced Ras-related protein 1, MGC:26290
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of RASD1

  • A549 cell infection with adenovirus engineered to express AGS1/RASD1 (Ad.AGS1) inhibited log phase growth in vitro and increased the percentage of cells undergoing apoptosis [1].
  • In clonogenic assays with NIH-3T3 murine fibroblast cells, the MCF-7 human breast cancer cell line and the human lung adenocarcinoma cell line A549, AGS1/RASD1 markedly diminished the number of G418-resistant colonies, whereas the Ras subgroup member K-Ras was without effect [1].
  • Expression of Dexras1 had no effect on expression of G(i)alpha species, but significantly impaired pertussis toxin-catalyzed ADP-ribosylation of membrane-associated G(i)alpha [2].
  • The analysis of survival curves revealed differences among the three groups; the RASD patients had lower survival probabilities than those of the RAminiD group, and significantly higher probabilities than those of the RAEB group [3].
 

High impact information on RASD1

 

Biological context of RASD1

  • The Ras-related protein AGS1/RASD1 suppresses cell growth [1].
  • Identification of a glucocorticoid response element in the 3'-flanking region of the human Dexras1 gene [5].
  • Activation of FPR by ligand (N-formyl-methionine-leucine-phenylalanine (f-MLF)) caused phosphorylation of endogenous Erk-1/2 that was reduced by co-expression of Dexras1 [2].
  • Dexras1 is a novel GTP-binding protein (G protein) that was recently discovered on the basis of rapid mRNA up-regulation by glucocorticoids in murine AtT-20 corticotroph cells and in several primary tissues [2].
  • Mutagenesis of Cys11 abolished the effect of NO donors on Dexras1, implicating this residue in the NO-mediated activation of Dexras1 [6].
 

Anatomical context of RASD1

  • Expression of Dexras1 also significantly decreased in vitro binding of GTPgammaS in f-MLF-stimulated membranes of cells co-transfected with FPR [2].
  • The present study was undertaken to examine the potential role of Dexras1 in the regulation of peptide hormone secretion in the AtT-20 corticotroph cell line [7].
  • GTP binding properties and the GTP to GDP ratio of wild-type and mutant Dexras1 proteins were examined in transiently transfected AtT-20 and COS-7 cells [7].
  • We proposed the new designations 'RA with severe dysplasia (RASD)' and 'RA with minimal dysplasia (RAminiD)'. In our criteria, RASD is considered present if a bone marrow (BM) examination shows Pseudo-Pelger-Huet anomalies of mature neutrophils > or =3% and/or micromegakaryocytes (mMgk) of megakaryocytes > or =10% in RA patients [3].
  • Anatomical variation in IHDs was classified according to the branching pattern of the right anterior and right posterior segmental duct (RASD and RPSD, respectively), and the presence or absence of the first-order branch of the left hepatic duct (LHD), and of an accessory hepatic duct [8].
 

Associations of RASD1 with chemical compounds

  • In addition, the in vivo and in vitro properties of AGS1 are consistent with it functioning as a direct guanine nucleotide exchange factor for Galpha(i)/Galpha(o) [9].
  • We describe the radiolabeling of S-nitrosylated cysteine residues in Dexras1 [6].
  • Dexras1/AGS-1, a steroid hormone-induced guanosine triphosphate-binding protein, inhibits 3',5'-cyclic adenosine monophosphate-stimulated secretion in AtT-20 corticotroph cells [7].
  • Heterologous sensitization of AC1 induced by persistent activation of D(2L) receptors was completely blocked by Dexras1 under basal and A23187-stimulated conditions [10].
  • We examined the ability of Dexras1 to modulate dopamine D(2L) receptor regulation of adenylyl cyclase (AC) type 1 in HEK293 cells [10].
 

Physical interactions of RASD1

 

Regulatory relationships of RASD1

  • Dexras1 is a steroid hormone-induced Ras family G protein that acts as a receptor-independent activator of signaling by Gi/o family heterotrimeric G proteins [11].
 

Other interactions of RASD1

  • These data indicate that AGS1/RASD1, a member of the Ras superfamily of small G-proteins that often promotes cell growth and tumor expansion, plays an active role in preventing aberrant cell growth [1].
  • Expression of Dexras1 alone resulted in a 1.9- to 4.9-fold increase in HA-Erk-2 activity; expression of the unliganded FPR alone resulted in a 6.2- to 8.1-fold increase in HA-Erk-2 activity [2].
  • Dexras1 mediated inhibition of adenylyl cyclase was blocked by treatment pertussis toxin or by co-expression of RGS4, but was not inhibited by with dominant-interfering (G203T or G204A) mutants of Gi alpha2 [11].
  • Dexras1/AGS1/RasD1 is a member of the Ras superfamily of monomeric G proteins and has been suggested to disrupt receptor-G protein signaling [10].
  • Dexras1 expression in human embryonic kidney 293 cells completely abolished dopamine D2 receptor-mediated potentiation of AC2 activity, which is consistent with previous reports of its ability to block receptor-mediated Gbetagamma signaling pathways [12].
 

Analytical, diagnostic and therapeutic context of RASD1

  • We have used yeast two hybrid analysis and co-immunoprecipitation studies in mammalian cells to demonstrate a direct interaction between AGS1 and the G(beta1) subunit of heterotrimeric G proteins [13].

References

  1. The Ras-related protein AGS1/RASD1 suppresses cell growth. Vaidyanathan, G., Cismowski, M.J., Wang, G., Vincent, T.S., Brown, K.D., Lanier, S.M. Oncogene (2004) [Pubmed]
  2. Dexras1/AGS-1 inhibits signal transduction from the Gi-coupled formyl peptide receptor to Erk-1/2 MAP kinases. Graham, T.E., Prossnitz, E.R., Dorin, R.I. J. Biol. Chem. (2002) [Pubmed]
  3. Refractory anemia with severe dysplasia: clinical significance of morphological features in refractory anemia. Matsuda, A., Jinnai, I., Yagasaki, F., Kusumoto, S., Minamihisamatsu, M., Honda, S., Murohashi, I., Bessho, M., Hirashima, K. Leukemia (1998) [Pubmed]
  4. NMDA receptor-nitric oxide transmission mediates neuronal iron homeostasis via the GTPase Dexras1. Cheah, J.H., Kim, S.F., Hester, L.D., Clancy, K.W., Patterson, S.E., Papadopoulos, V., Snyder, S.H. Neuron (2006) [Pubmed]
  5. Identification of a glucocorticoid response element in the 3'-flanking region of the human Dexras1 gene. Kemppainen, R.J., Cox, E., Behrend, E.N., Brogan, M.D., Ammons, J.M. Biochim. Biophys. Acta (2003) [Pubmed]
  6. Nitrosopeptide mapping: a novel methodology reveals s-nitrosylation of dexras1 on a single cysteine residue. Jaffrey, S.R., Fang, M., Snyder, S.H. Chem. Biol. (2002) [Pubmed]
  7. Dexras1/AGS-1, a steroid hormone-induced guanosine triphosphate-binding protein, inhibits 3',5'-cyclic adenosine monophosphate-stimulated secretion in AtT-20 corticotroph cells. Graham, T.E., Key, T.A., Kilpatrick, K., Dorin, R.I. Endocrinology (2001) [Pubmed]
  8. Anatomic variation in intrahepatic bile ducts: an analysis of intraoperative cholangiograms in 300 consecutive donors for living donor liver transplantation. Choi, J.W., Kim, T.K., Kim, K.W., Kim, A.Y., Kim, P.N., Ha, H.K., Lee, M.G. Korean journal of radiology : official journal of the Korean Radiological Society. (2003) [Pubmed]
  9. Activation of heterotrimeric G-protein signaling by a ras-related protein. Implications for signal integration. Cismowski, M.J., Ma, C., Ribas, C., Xie, X., Spruyt, M., Lizano, J.S., Lanier, S.M., Duzic, E. J. Biol. Chem. (2000) [Pubmed]
  10. Dexras1 blocks receptor-mediated heterologous sensitization of adenylyl cyclase 1. Nguyen, C.H., Watts, V.J. Biochem. Biophys. Res. Commun. (2005) [Pubmed]
  11. Dexras1 inhibits adenylyl cyclase. Graham, T.E., Qiao, Z., Dorin, R.I. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  12. Dexamethasone-induced Ras protein 1 negatively regulates protein kinase C delta: implications for adenylyl cyclase 2 signaling. Nguyen, C.H., Watts, V.J. Mol. Pharmacol. (2006) [Pubmed]
  13. Specific in vivo binding of activator of G protein signalling 1 to the Gbeta1 subunit. Hiskens, R., Vatish, M., Hill, C., Davey, J., Ladds, G. Biochem. Biophys. Res. Commun. (2005) [Pubmed]
 
WikiGenes - Universities